Degenerative Muscle Disorders Flashcards
1
Q
what are synovial joints
A
movable joints
2
Q
what are synovial joints composed of
A
outer fibrous capsule
interior synovial fluid
articular cartilage
synovial fluid
3
Q
what is the function of a synovial joint
A
provide smooth surface and lubrication at the place where bones come together to prevent friction
4
Q
what is OA
A
degeneration of joints caused by aging and stresses
5
Q
what is causing in increase in OA
A
obesity and aging
6
Q
what joints are most commonly affected by OA
A
cervical spine
lumbosacral spine
hip
knee
hand
first metatarsal phalangeal joint
spare wrist, elbow, ankle
7
Q
what are the risk factors for OA
A
obesity
aging
hx of team sports, trauma/overuse
heavy occupational work
misalignment (women have wider hips)
8
Q
etiology of OA
A
degradation of cartilage due to
- excessive loading of healthy joints
- normal loading of previously injured joints
stress applied at wt bearing joints
9
Q
what is the patho of OA
A
- pressure wears away cartilage, exposing subchondral bone that results in the development of cysts
- cysts move through cartilage inc damage
- chondrocytes will synthesize proteoglycans to repair cartilage which results in swelling from excess fluid
- localized inflammation occurs inc damage again
- osteoblasts are activated creating bony spurs and inc thickness of synovial fluid
10
Q
as OA progresses, what happens to proteoglycans
A
they decrease
11
Q
what does the loss of cartilage lead to
A
narrowing of the joint space
12
Q
what are the 3 major things that happen with OA
A
- bone: formation of bone spurs
- cartilage: dec number of chondrocytes, so dec in cartilage repair
- synovial fluid: thickens due to the inc in inflammatory response
13
Q
what are osetophytes
A
small bony projection that develop along the rim of bone adjacent to cartilage loss
14
Q
what is the hallmark of OA
A
osteophytes
15
Q
what are the sx of OA
A
deep achy joint pain: inc w exertion, better at rest
pain during colder weather
stiffness in AM
crepitus w moving
joint swelling
altered gait
limited range of motion
16
Q
what is the physical exam for OA
A
joint deformities and tenderness
dec ROM
fingers (late stage)
- herbeden’s nodes
- bouchard’s nodes
17
Q
what are herbeden’s nodes
A
swelling at the distal interphalangeal joint
18
Q
what are bouchard’s nodes
A
swelling at proximal interphalangeal joint
19
Q
what are OA treatment goals
A
manage pain
maintain mobility
minimize disability
20
Q
what pharm is used for OA
A
midl to moderate pain
- acetaminophen
- topical capsaicin
- NSAIDS
moderate to severe pain
- NSIADS (rx strength)
- NSIADS + colchicine
- Tylenol + tramadol
- opioids
- steroid injections
21
Q
what is the MOA of NSAIDS
A
reduce the production of prostaglandins which are what promotes inflammation, pain, fever
22
Q
what organ and system do NSAIDs potentially hurt the most
A
kidney
GI risk for bleeding
23
Q
NSAIDs and the risk for bleeding
A
- inc risk in older people
- use caution if have had previous GI bleed or currently using anticoags
- contraindicated for ppl w PUD
24
Q
what are additional pharm therapies often used for OA
A
- intra articular injection of glucocorticoids
- dietary supplements: chondroitin sulfate, glucosamine
- artifical joint fluid w hyaluronic acid
25
what is glucosamine sulfate
naturally occurring compound in body that helpd maintain cartilage health
- dec amount in body w age
26
what is chondroitin sulfate
naturally occurring chemical in cartilage that *might* slow doen cartilage breakdown
27
what is DDD
degenerative disc disease
- causes pain, motor weakness, neuropathy
28
where does DDD typically occur
lumbar and cervical spine
29
what is the patho of degenerative disc disease
intervertebral discs become dehydrated w age causing vertebral bones to become compressed which impinges on entering and exiting nerves
- causes dysfunction of motor and sensory spinal nerves impeding on movement and sensation of extremities
- weakness and paresthesia
30
what are s/s of lumbar DDD
pain in lower back that radiates down back of legs
pain in buttock/thighs
pain that worsens when sitting, bending, lifting, twisting
pain that is minimized when walking, changing positions, lying down
numbness, tingling, foot drop, weakness
31
what are the s/s of cervical DDD
chronic pain that radiates to shoulders and down arms
weakness and tingling/weakness in arm/hand
32
what is rheumatoid arthritis
systemic, auto immune, inflammatory condition of the synovium that causes
- pain
- limitation of movement
- destruction or erosion of joints, ligaments, muscles
33
what type of reaction are rheumatoid arthritis and lupus
type III
34
why does RA occur
unknown
- genetic factors and env links
- maybe an inappropriate immune response to joint injury
35
what are risk factors of RA
40-60
women
tobacco use
36
what is the patho of RA
autoimmune attack on synovial tissue
- cells activated are lymphocytes and macrophages which produce RH
37
what is RF
rheumatoid factor
- auto antibody against the body's own antibody - IgG which forms immune complexes and activates complement --> deposits into tissue and causes damage
38
what is RA diagnosed
measure serum levels of RF
39
what happens as RA progresses
intensifying inflammatory response causes
- cartilage destruction by osteoclasts
- pannus formation
40
what is pannus
an extra growth of the joints that is vascularized and able to get nutrients
- causes: bone erosion, bone cysts, fissure development
41
what are early clinical manifestations of RA
vague
- fatigue, anorexia, generalized stiffness
42
what are later manifestations of RA
symmetrical pain, stiffness, motion limitations
inflammation: heat, swelling, tenderness
43
what are the advanced characteristics of RA
deformities and disabilities
joint subluxation
44
what is joint subluxation
the bone gets displaced bc the joint loses contact with articulating surface
45
how is RA systemic?
causes fatigue and malaise
- potentially affects all/any body systems
most common
- rheumatoid nodules
- sjogrens syndrome
46
what are rheumatoid nodules
immune mediated granulomas that develop around inflamed joints and in lungs
- subcutaneous and firm, necrotic core
- sometimes painful
47
what are the goals of pharm for RA
relieve pain and swelling
slow or stop disease progression
48
what pharm is used for RA
NSAIDs: immediate relief
Glucocorticoids: short term only
DMARDS
49
what is lupus
autoimmune inflammatory disease that attacks the DNA's own body
- multiple organ system
- acute flare up
- unpredictable
50
what are the two forms of lupus
- discoid: disease targets the skin
- systemic: disease targets internal organs
51
what type of sensitivity is lupus
type III
52
what are the predisposing factors for SLE
genetic factors
female
20-40
african american
env triggers like UV rays
allergy to abx
hormonal factors --> oral contraceptives
tobacco use
53
what is the SLE patho
B lymphocytes are hyperactive and produce antibodies called antinuclear antibody (ANA)
- when ANA are activated they attack DNA
- form immune complexes in tissues causing an inflammatory response that destroys tissue
54
what are SLE manifestations (broad)
extreme fatigue
photosensitivity
butterfly rash
fever
wt change
unusual hair loss
edema
raynauds
55
what are the multisystemic manifestations of SLE
CNS: h/a, dizzy, seizures, stroke
lungs: pleuritis, pleural effusions
heart: myocarditis, endocarditis
kidneys: nephritis
blood vessels: vasculitis
blood: anemia, leukopenia, thrombocytopenia, blood clots
Joints: arthritis
56
what is a SLE flare
SLE characterized by exacerbations and remissions
- flare = acute exacerbation
57
what are the warning signs of flares
fatigue
pain
headache
58
what are ways to prevent flares
recognize warning signs and avoid triggers like
- sunlight exposure
- infection
- abruptly stopping meds
- stress
59
what is sjogren syndrome
autoimmune destruction of any moisture producing gland
- enlarged gland with dec function
- lacrimal gland is dec tears
- salivary gland is dec papilla
60
what is the pharm used for SLE
relieve pain and swelling
slow or stop disease prevention
- NSAIDs, glucocorticoids, DMARDS
61
why are corticosteroids used for RA and SLE
rapid suppression of inflammation
- aids if sx not relieved by NSAIDs or w/ a flare up
- not for long term therapy
62
what is the class of methotrexate
DMARD, antineoplastic, anti-rheumatic
- folic acid antimetabolite
63
what is the moa for methotrexate
immunosuppressive
64
how is methotrexate administered
PO or SQ/IV weekly
65
what are side effects of methotrexate
GI
bone marrow suppression
shortened life expectancy (CVD and cancer)
liver toxicity
*destroys rapidly producing cells*
66
what are nursing implications for methotrexate
11 black box warnings
folic acid supplement is necessary
no alc, pregnant
teach s/s of infection and no notify provider
67
what is hydroxychloroquine class
DMARD, antimalarial, antirheumatic agent
68
what is the moa of hydroxychloroquine
unknown, maybe have anti inflammatory properties
69
what is the indication of hydroxychloroquine
slow the progression of RA when used w another DMARD
- often alone or combo w methotrexate
70
what are the side effects of hydroxychloroquine
retinopathy
71
what are the similarities between RA and SLE
- autoimmune
- systemic inflammation
- multiple body systems
- pharm
72
what are the differences between RA and SLE
RA affects joints and sometimes organs
SLE affects organs and sometimes joints
73
what is gout
type of arthritis caused by the deposition of urate salts/crystals into the synovial fluid
- acute and painful inflammation
74
what is chronic tophaceous gout?
advanced stage of gout characterized by white nodules composed of uric acid
75
what is uric acid
waste product from purine metabolism
76
what does purine contain
nitrogen containing compound
77
what are sources of purines
alcohol
organ meat like liver
red meat
seafood, shell fish
78
where are uric acid typically excreted by
kidneys
79
what are predisposing factors of gout
male
genetics
diet
obesity
diuretic therapy + kidney insufficiency
80
what is gout pathogenesis
elevated uric acids levels which accumulate in the body fluids
formation of urate crystals which deposit around the joints causing inflammation
result is gouty arthritis
81
what are gouty arthritis manifestations
pain: intense, great toe, early manifestations
inflammation: edema, tenderness, redness
fever
malaise
82
what are complications of gouty arthritis
urate kidney stones
83
what is the pharm for gout
acute
- NSIADs
- corticosteroid therapy
- colchicine
prophylactic
- allopurinol
- colchicine
- probenecid
84
what is allopurinol class
antigout
85
what is the moa of allopurinol
inhibits production of uric acid
86
what is the therapeutic use for allopurinol
gout prophylaxis
87
what are the adverse effects of allopurinol
rash
88
what interactions are we concerned for with allopurinol
hypoglycemic agents: causes inc insulin, which dec glucose
warfarin: inc risk of bleeding
89
what are the nursing implications of allopurinol
- can cause gastric irritation so take with food or milk
- monitor urine uric acid level and glucose
- takes 2-6 wks to see improvement
90
what class is colchicine
anti inflammatory, anti gout
91
what is the moa of colchicine
unknown, thought to inhibit leukocyte infiltration and disrupt cell division
92
what is the therapeutic use of colchicine
gout flare ups and prophylaxis
93
what are the adverse effects of colchicine
GI problems bc they are rapid reproducing cells also
- typically the first sign of drug toxicity so stop immediately
94
what are nursing considerations for colchicine
usually given oral
contraindicated for renal disease
avoid grapefruit, alc, B12
check for other interactions: CYP3A4 inhibitors, anoxin, statins, etc
95
what class is probenecid
uricosuric agent
96
what is the moa of probenecid
inhibits reabsorption of uric acid in the kidneys, promoting excretion
97
what are the therapeutic uses of probenecid
treats hyperuricemia with gout
98
what are the side effects of probenecid
Gi upset
dizzy
h/a
kidney/liver impairment --> hematuria, color changes, output changes, wt gain, n/v
lots of drug interactions
